Carbon disulfide (CS2), a common industrial solvent, produces a variety of effects with continued exposure, ranging from producing an irritating odor to causing a biochemical imbalance in the brain and, eventually, to producing central and/or peripheral neuropahty. The olfactory aversive stimulus produced by CS2 is often the primary signal of overexposure. However, chronic low-level exposure may obviate this protective mechanism and toxicity from excessive inhalation may result. Furthermore, CS2 has been shown to inhibt the enzyme dopamine-Beta-hydroxylase (DBH), resulting in decreased brain norepinephrine (NE) levels. The aim of this proposal is to investigate the effect of this brain biochemical (i.e., NE) on the production of aversiveness to CS2 and upon habituation that may be produced to his aversiveness. The methodology will include ltraining rats in a vapor chamber using an operant conditioning paradigm to turn off (i.e., escape) or actively avoid the presentation of CS2 vapors using control procedures to insure that non-associative confounds are minimized. Different concentrations of CS2, then, will be presented after the presence of absence of chronic CS2 exposure to determine olfactory escape and avoidance (detection) tresholds, and how these thresholds may be affected by chronic CS2 exposure (i.e, habituation). Other pharmocological agents that decrease NE levels will be utilized in CS2-trained rats, both acutely and chronically, to determine regional brain catecholamine level mediation of the aversiveness of, and habituation to, the CS2 odor. In addition, the replenishment of central NE stores will be examined in an attempt to reverse habituation. Lastly, indices of central and peripheral neuropathy will be examined to measure possible intercorrelations between neuropathy, biochemical alterations and behavioral performace. Since CS2 is a common industrial solven, "poisoning" by CS2 represents a real health problem. Hence, the study of CS2 effects involves the disciplines of pharmacology, since CS2 is a DBH inhibitor; toxicology, since it can produce frank neuropathy; and environmental/occupational health, due to its widespread industrial use.